Synta Pharmaceuticals Corp. (SNTA)

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Synta Pharmaceuticals Corp. (SNTA)

Barclays Global Healthcare Conference

March 12, 2013 3:45 pm ET


George Farmer - Vice President of Corporate Development


Ying Huang - Barclays Capital, Research Division


Ying Huang - Barclays Capital, Research Division

My name is Ying Huang. I'm the U.S. biotech analyst here at Barclays. So very pleased to introduce my next presenting company in biotech, which is Synta Pharmaceuticals. And then also I'm very pleased to introduce the speaker on behalf of Synta, George Farmer, who is the VP of Corporate Development at Synta. So with that, let me turn the podium to George.

George Farmer

Thanks very much, Ying. Ying and I have known each other a long time. I will be making some forward-looking statements. Please refer to our website and SEC filings for further detail.

Synta Pharmaceuticals was formed out of a joint venture between 2 Japanese companies back in 2002. Our CEO, Safi Bahcall, led a management-led buyout. Public went company -- the company went public in 2007. Brought 120 employees in Lexington, Massachusetts with a small molecule pipeline of a number of different drugs. And importantly, we own a 100% of the worldwide rights to our pipeline, which is shown here. I will spend all of my time today talking about our lead compound, ganetespib, which is an Hsp90 inhibitor, which is being evaluated in a broad GALAXY program of 2 randomized trials as well as other genetically-defined settings in ALK+ non-small cell lung cancer and metastatic breast cancer. And we have over 20 clinical trials ongoing with collaborators at cooperative groups in various institutions.

Ganetespib is a novel molecule that's highly targeted to a very specific protein, but has shown to have a very broad applicability and is very active across many different tumor types. We've treated over 600 patients with this drug in over 20 clinical trials and have seen very encouraging signs of activity, both as a single agent and in combination with other cancer drugs. We believe the drug is poised to serve some very large markets. And again, we own 100% of the worldwide rights.

The first indication that we see ganetespib ultimately being approved for is in non-small cell lung cancer in the second-line treatment setting, specifically for adenocarcinoma patients. We're estimating about 160,000 new cases of adenocarcinoma in the major territories. Assuming a modest penetration rate and pricing of current oncology drugs, we see the opportunity alone in second-line non-small cell lung cancer as being in excess of $2 billion a year.

Our GALAXY program is consisted of 2 randomized clinical trials, both effectively designed the same, evaluating ganetespib in combination with standard of care second-line chemotherapy. We reported interim analyses from this GALAXY-1 trial at September -- I'll touch on the results later on in the presentation -- and expect to have 6-month overall survival data at -- for presentation, hopefully, at ASCO, in the June time frame, then some other data points later on from GALAXY-1. In parallel, we're initiating the GALAXY-2 confirmatory Phase III trial which will ultimately be about 500 patients and we plan to have some data readouts from that study next year.

This is an illustration of our -- of a concept that came out of Forbes Magazine from an article on cancer drug development last year. Showing that there are about 500 different small molecule tyrosine kinase inhibitors in clinical development, preclinical development or have launched today. A lot of them go after the same targets, which have been validated in the clinic already and also in preclinical molecules. But this really just illustrates how there's a lot of copycats out there. A lot of people are chasing after the same targets with molecules that are not really very well differentiated in our view. What's special about ganetespib is while we are a targeted therapy, the target that we're going after is a very specific one. And by virtue of going after this very specific target that has multiple -- capable of multi-silence and multiple oncogenic pathways at once, we can achieve this activity in a very clean manner but having a very wide collection of specs. This is in contrast to the target therapeutics that are on the market like GLEEVEC, Herceptin and Tarceva, which are very -- have very specific targets and have very specific pathways; and in contrast to the dirtier TKIs and broad chemotherapies which have these wide effects on multiple pathways.

Hsp90, the target for ganetespib, is a chaperone protein, shown there in blue. And the chaperones in the cells are required for maintaining the integrity of a number of different client proteins that are involved in cell growth and tumorigenesis. A lot of those are listed down there on the left, some very familiar names and common targets by the pharmaceutical and biotech industry. When Hsp90 is inhibited by ganetespib, the client and the chaperone dissociate and the client's integrity effectively falls apart and is shunted into the proteasome pathway and degraded. So in contrast to kinase inhibitors, which effectively shut off the activity of a specific kinase, inhibition of Hsp90 ganetespib leads to the elimination of the kinase in the cell.

Here is an example of that, this is a western blot on the right, showing that ganetespib can have simultaneously -- simultaneous broad inhibitory activity on a number of different kinase -- kinases involved in tumorigenesis.

We see development of ganetespib in sort of a two-pronged approach. One is as a monotherapy in genetically defined diseases where the clients are well known and known to be important drivers of tumorigenesis. And the other is in combination with chemotherapeutic agents that are either targeted therapies or radiation, or we think that the addition of ganetespib is affecting -- is sensitizing the activities of these other treatment modalities and is inhibiting angiogenesis metastasis, mechanisms of DNA repair and resistance simultaneously, and enabling these other therapeutics to have more of a cytotoxic effect.

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